Aroclor 1254 as a 2,3,7,8-tetrachlorodibenzo-p-dioxin antagonist in mice

Chemosphere ◽  
1989 ◽  
Vol 18 (1-6) ◽  
pp. 709-714 ◽  
Author(s):  
S. Safe ◽  
R. Bannister ◽  
D. Davis ◽  
J.M. Haake ◽  
T. Zacharewski ◽  
...  
Keyword(s):  
Aroclor 1254 ◽  
Tetrachlorodibenzo P Dioxin

scholarly journals Dose-dependent acinar induction of cytochromes P450 in rat liver. Evidence for a differential mechanism of induction of P450IA1 by β-naphthoflavone and dioxin

1991 ◽  
Vol 277 (2) ◽  
pp. 577-580 ◽  
Author(s):  
R G Bars ◽  
C R Elcombe
Keyword(s):  
Western Blotting ◽  
Rat Liver ◽  
Low Dose ◽  
Cytochromes P450 ◽  
Aroclor 1254 ◽  
Hepatic Expression ◽  
Differential Mechanism ◽  
Tetrachlorodibenzo P Dioxin ◽  
High Doses ◽  
Dose Dependent

Rats received various doses of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), Aroclor 1254 (ARO), beta-naphthoflavone (BNF) or phenobarbital (PB), and the hepatic expression of cytochromes P450IA1 and/or P450IIB1/IIB2 was analysed by immunohistochemistry and Western blotting. A clear heterogeneous acinar induction of IA1 was detected when a low dose of TCDD, ARO or BNF was administered. When a low dose of TCDD or ARO was administered, IA1 was found to be induced primarily in hepatocytes located in acinus zone 3, whereas when a low dose of BNF was administered, IA1 was found to be preferentially induced in hepatocytes located in acinus zone 1. A clear zonal induction of IIB1/IIB2 was also observed when a low dose of PB or ARO was administered. Both compounds induced IIB1/IIB2 preferentially in hepatocytes located in acinus zone 3. When rats were administered high doses of TCDD, ARO, BNF or PB there was no zonal pattern of induction of IA1 or IIB1/IIB2; instead, a pan-acinar induction of these enzymes was observed. These results indicate that the overall hepatic concentration of IA1 or IIB1/IIB2 is merely dependent on the proportion of ‘induced hepatocytes’ within the acinus, which in turn depends on the dose of the inducer.

Aroclor 1254 as an antagonist of the teratogenicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin

1987 ◽  
Vol 38 (3) ◽  
pp. 299-306 ◽  
Author(s):  
J.M. Haake ◽  
S. Safe ◽  
K. Mayura ◽  
T.D. Phillips
Keyword(s):  
Aroclor 1254 ◽  
Tetrachlorodibenzo P Dioxin

Aroclor 1254 as a 2,3,7,8-tetrachlorodibenzo-p-dioxin antagonist: Effects on enzyme induction and immunotoxicity

Toxicology ◽  
1987 ◽  
Vol 46 (1) ◽  
pp. 29-42 ◽  
Author(s):  
R. Bannister ◽  
D. Davis ◽  
T. Zacharewski ◽  
I. Tizard ◽  
S. Safe
Keyword(s):  
Enzyme Induction ◽  
Aroclor 1254 ◽  
Tetrachlorodibenzo P Dioxin

An Investigation of the Effects of Curcumin on the Changes in the Central Nervous System of Rats Exposed to Aroclor 1254 in the Prenatal Period

2018 ◽  
Vol 17 (2) ◽  
pp. 132-143 ◽  
Author(s):  
Mehmet Eray Alcigir ◽  
Halef Okan Dogan ◽  
Begum Yurdakok Dikmen ◽  
Kubra Dogan ◽  
Sevil Atalay Vural ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Neuron Specific Enolase ◽  
Control Group ◽  
Albino Rats ◽  
Prenatal Period ◽  
Aroclor 1254 ◽  
Rat Pups ◽  
Tunel Reaction ◽  
The Central Nervous System

Background & Objective: Aroclor 1254 is a widespread toxic compound of Polychlorinated Biphenyls (PCBs), which can create significant nervous problems. No remedies have been found to date. The aim of this study was to reveal the damage that occurs in the central nervous system of rat pups exposed to Aroclor 1254 in the prenatal period and to show the inhibiting effect of curcumin, which is a strong anti-oxidant and neuroprotective substance. Method: The study established 3 groups of adult female and male Wistar albino rats. The rats were mated within these groups and the offspring rats were evaluated within the group given Aroclor 1254 only (n=10) and the group was given both Aroclor 1254 and curcumin (n=10) and the control group (n=10). The groups were compared in respect of pathomorphological damage. The immunohistochemical evaluation was made of 8-hydroxdeoxyguanosine (8-OHdG), 4-hydroxynoneal (4HNE), myelin basic protein (MBP) expressions and TUNEL reaction. The biochemical evaluation was made of the changes in the TAS-TOS and Neuron Specific Enolase (NSE) levels. Damage was seen to have been reduced with curcumin in the 8OHdG and TUNEL reactions, especially in the forebrain and the midbrain, although the dosage applied did not significantly change TAS and TOS levels. Consequently, it was understood that Aroclor 1254 caused damage in the central nervous system of the pup in the prenatal period, and curcumin reduced these negative effects, particularly in the forebrain and the midbrain. Conclusion: It was concluded that curcumin could be a potential neuroprotective agent and would be more effective at higher doses.

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